Body mass index and gastrointestinal inflammation: Bio-molecular pathophysiology

Figure 4 Dysbiosis–endotoxemia–inflammation–barrier dysfunction cycle induced by a high-fat diet. Obesity-associated dysbiosis stimulates lipopolysaccharides translocation and tumor necrosis factor alpha/nuclear factor kappa B triggering, with ↓zonula occludens-1, ↑paracellular permeability, and ↓mucin production. At the same time, ↓NOD-like receptor family pyrin domain containing 6-interleukin-18 signaling and ↓aryl hydrocarbon receptor activity damage mucosal integrity, and reduced ethanolamine availability (a phosphatidylethanolamine precursor) may contribute to ↓phospholipid synthesis, increasing epithelial disruption. AHR: Aryl hydrocarbon receptor; IL: Interleukin; LPS: Lipopolysaccharides; NF-κB: Nuclear factor kappa B; TNF-α: Tumor necrosis factor alpha; ZO-1: Zonula occludens-1; NLRP6: NOD-like receptor family pyrin domain containing 6.